It has been postulated that the aberrant projection of sympathetic axo
ns to individual primary sensory neurons may provide the morphological
basis for pain-related behaviors in rat models of chronic pain syndro
me, Since nerve growth factor (NGF) can elicit the collateral sproutin
g of noradrenergic sympathetic terminals, it might be predicted that N
GF plays a role in mediating the sprouting of sympathetic axons into s
ensory ganglia. Using a line of transgenic mice overexpressing NGF amo
ng glial cells, it was first found that trigeminal ganglia from adult
transgenic mice possessed significantly higher levels of NGF protein i
n comparison to age-matched wildtype mice; as well, detectable levels
of NGF mRNA transgene expression were present in both the ganglia and
brain stem. Within the trigeminal ganglia, a small proportion of the s
ensory neuronal population stained immunohistochemically for NGF; a hi
gher percentage of NGF-positive neurons was evident in transgenic mice
, New sympathetic axons extended into the trigeminal ganglia of transg
enic mice only and formed perineuronal plexuses surrounding only those
neurons immunostained for NGF, In addition, such plexuses were accomp
anied by glial processes from nonmyelinating Schwann cells, From these
data, we propose that accumulation of glial-derived NGF by adult sens
ory neurons and its putative release into the ganglionic environment i
nduce the directional growth of sympathetic axons to the source of NGF
, namely, the cell bodies of primary sensory neurons. (C) 1998 John Wi
ley & Sons, Inc.